Cancer is a disease having many etiologies encompassing environmental toxins, disease, microbiological infections, and/or genetic predispositions. As such, each causative factor can, and does, result in a different type of cancer that usually manifests in a different biological tissue. As a result, no one therapeutic approach has been identified that has been effective at slowing or preventing the progression of a large percentage of different cancerous types. The only commonality that is currently recognized between all cancer diseases is manifested by an uncontrolled cellular growth rate.
Current theories related to epithelial cell growth predicts a regulatory pathway that balances the effects of mitogenic stimuli and apoptosis. Croker et al., “Cancer stem cells: implications for the progression and treatment of metastatic disease” J Cell Mol Med 2008, 12:374-390; and Rodriguez-Nieto et al., “Role of alterations in the apoptotic machinery in sensitivity of cancer cells to treatment’ Curr Pharm Des 2006, 12:4411-4425. Apoptosis is believed to be a homeostatic process orchestrated by the host's genome of selective cell deletion without stimulating inflammatory response. Wyllie et al., “Cell death: the significance of apoptosis” Int Rev Cytol 1980, 68:251-306; Ellis et al., “Mechanisms and functions of cell death” Annul Rev Cell Biol 1991, 7:663-698; and Fawthrop et al., “Mechanisms of cell death” Arch Toxicol 1991, 65:437-444. Dysregulation of apoptotic cell-death has been implicated in states of disease and in the neoplastic transformation. Soti et al., “Apoptosis, necrosis and cellular senescence: chaperone occupancy as a potential switch” Aging Cell 2003, 2:39-45; and Renvoize et al., “Apoptosis: identification of dying cells” Cell Biol Toxicol 1998, 14:111-120. Present anti-cancer therapies all share a common problem in that normal non-cancerous cells are susceptible to the various treatments (i.e., for example, radiation and/or chemotherapy).
What is needed in the art is a single unified approach to cancer treatment that is directed at the common unifying mechanism of uncontrolled growth rates. One approach having a potential for success is related to re-balancing cell proliferation/apoptosis homeostasis such that apoptosis predominates, such that the cell proliferation/apoptosis homeostasis is not affected in non-cancerous tissues.